Clapham J C
J Cardiovasc Pharmacol. 1984 Jul-Aug;6(4):668-71. doi: 10.1097/00005344-198407000-00018.
In spontaneously hypertensive rats (SHR), oral antihypertensive doses of nifedipine exert potent inhibitory effects on pressor responses elicited by xylazine and angiotensin II, and by stimulation of the complete sympathetic outflow, suggesting that extracellular calcium is a prerequisite for responses to these stimuli. On the other hand, only those pressor responses to low doses of phenylephrine are affected by nifedipine, suggesting less dependence of phenylephrine on extracellular calcium. The results, therefore, indicate that postsynaptic alpha-adrenoceptors mediating pressor responses to neuronally released noradrenaline and phenylephrine may differ in their dependence on extracellular calcium, although they are both considered to be of the alpha 1-subtype. The evidence also suggests that this ability of nifedipine to inhibit pressor responses to neuronally released noradrenaline, as well as pressor responses to angiotensin II, contributes to the efficacy of this drug as an antihypertensive in SHR.
在自发性高血压大鼠(SHR)中,口服降压剂量的硝苯地平对由赛拉嗪和血管紧张素II以及完全交感神经传出刺激引发的升压反应具有强大的抑制作用,这表明细胞外钙是对这些刺激作出反应的先决条件。另一方面,只有对低剂量去氧肾上腺素的升压反应受硝苯地平影响,这表明去氧肾上腺素对细胞外钙的依赖性较小。因此,结果表明,介导对神经元释放的去甲肾上腺素和去氧肾上腺素的升压反应的突触后α-肾上腺素能受体对细胞外钙的依赖性可能不同,尽管它们都被认为是α1亚型。证据还表明,硝苯地平抑制对神经元释放的去甲肾上腺素的升压反应以及对血管紧张素II的升压反应的这种能力,有助于该药物作为SHR降压药的疗效。